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Patho > Weak Points Midterm > Flashcards

Weak Points Midterm Flashcards

1
Q

Incubation

A

Pathogen replicates no symptoms rapid or slow onset

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2
Q

Prodromal

A

Symptoms become detectable

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3
Q

Acute

A

Tissue damage inflm dt toxins from pathogens being released at lysis. Most severe symptoms

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4
Q

Convalescent

A

Body continues to rid pathogen inf plateaus symptoms decrease

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5
Q

Resolution

A

Pathogen absolutely eliminated no present symptoms

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6
Q

Dysplasia

A

Diff shape size arrangement cells. Faulty tissue. Can progress to anaplasia. Increased mitosis index. Pre cancerous

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7
Q

Necrosis

A

Cell death dt injury. Abnormal. Initiates inflammatory response.

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8
Q

Fibrinous exudate

A

Lots of fibrinogen and other components. Sticky mesh

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9
Q

Membranous exudate

A

Dev of mucous membrane. Necrotic cells in fibropurulent exudate

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10
Q

CRP

A

Hepatic protein produced in response to inflm. Serum marker. Has a role via complement. Increased levels in atherosclerosis

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11
Q

NSAIDS for tx of inflm

A

Decreases prostaglandin synthesis which decreases pain

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12
Q

Steroidal anti inflammatory for tx inflm

A

Decrease cap perm, decrease wbc and mast cells to site, decrease prostaglandin and histamine release

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13
Q

Shock is

A

Acute hypoperfusion leading to hypoxia

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14
Q

Anaphylactic shock

A

Dt severe allergic reaction. Systemic edema dt increased perm. Fluid lost from blood to tissues = hypovolemia = circulatory failure

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15
Q

Mediators released by mast cells during anaphylaxis do what

A

Work on SM of bvs and resp tract. Cause vasoconstriction of resp tract = broncho spasm

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16
Q

Septic shock dt

A

Severe infection. Becomes systemic dt multiple infections and many mediators being released and circulating throughout body.

Vasodilatory = hypotension = hypoperfusion = shock

Causes systemic inflm and multiple organ dysfx

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17
Q

Aneurysms caused by

A

Degenerative change in BV wall (congenital defects, trauma, atherosclerosis) causing localized dilation of an artery

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18
Q

Common sites for aneurysms

A

Abd/thoracic aorta, femoral artery, Iliad and popliteal

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19
Q

Saccular
Fusiform
Dissecting

A

1 sided
Entire circumference
Blood flows Btwn 2 layers bulge

20
Q

Complications of aneurysms

A

Pressure to surrounding
Rupture hemmorhagging
Clotting - thrombosis = distal emboli satin

21
Q

Tx of angina

A

Decreased activity, nitroglycerin

22
Q

When is nitro used

A

Tx of angina, not used DURING AN MI, but used post MI to prevent risk of having another

23
Q

If unstable plaque ruptured

A

Thrombosis- platelets aggregate - PG release - vasopasm

24
Q

Stable angina causes what kind of pain

A

Transient

25
Q

Variant/vasopastic angina

A

Not caused by atherosclerosis but a thrombus. Happens at rest nocturnally. No known cause. Dt spasm of coronary artery

26
Q

2 types of MI

A

Subendocardial
(Inner 1/3-1/2 v wall. Distal occlusion in coronary branches)

Transmural
(Entire v wall. 1 proximal artery occluded)

27
Q

DX of mi

A

ECG abnormalities (ST seg, T wave inversion)

Myoglobin

CKMB (cardiac muscle specific ez)

Troponin I & T (elevates first)

28
Q

Meds to tx mi

A

Thrombolytics (break up clot, pieces circulate)
Antiarrythmics (bring rhythm back that was lost dt met acidosis)
Anticoagulants (prevents platelet aggregation, clot can not grow)

29
Q

Cardiomyopathy

A

Cardiac muscle disorder

30
Q

Hypertrophic cardiomyopathy

A

Excessive hyper trophy of CM in v wall.

Inc wall thickness dec chamber size dec vol into chamber

Thick IV septum

31
Q

Hyp. Cardiomyopathy et

A

50% autosomal dominant (genetic) 50% idiopathic

32
Q

Symptoms of hyp cardiomyopathy if they occur are

Tx

A

Dyspnea, angina, syncope, palpitations, sudden death

Negative inotropes, alcohol septal ablation

33
Q

Dilated/congestive cardiomyopathy

A

V wall enlargement (heart walls stretched)

Weak contraction

Decreased stroke volume

Alcohol abuse implicated

34
Q

Restricted cardiomyopathy

A

Rigid v walls. Muscle cannot contract or relax, incomplete filling - dec CO. Leads to CHF

35
Q

Arrhythmia occur in only diseases hearts. t or f

A

F

Also in normal hearts

36
Q

Et of arrhythmias

A

Heart defects, ischemia, mi, drugs, fluid/electrolyte imbalance (effects resting membrane potential), acid base imbalance

37
Q

Atrial flutter

A

Reg rhythm, increased rate. Atrial tachycardia 300 Bpm. Ventricles tachy 150. A:v 2:1

38
Q

Atrial fibrillation

A

Spontaneous episode of irregular chaotic contractions 400-600 Bpm. ventricles irregular and rapid 80-180

39
Q

Heart block

A

Atria fill and empty properly, but conduction of impulses from a to v abn or absent

40
Q

Degrees of heart block

A

1st: delayed connection. Reg rhythm. Impulse passed but delayed
2nd: some signals conducted, some not. Intermittent failure of conduction
3rd: no conduction Btwn a and v. Nodal cells in v create new pacemaker. A and v have separate rhythms.

41
Q

Ventricular fibrillation

A

Quivering of v. No cont. can cause death in minutes

42
Q

Tx of arrhythmias

A

Based on type and if needed.

Drugs
Defibrillation (clears all electrical activity in heart to reinstate normal sinus rhythm)
Sx (ablation of infarcts area that is causing arrhythmia, or pacemaker)

43
Q

Valvular disease et

A

Age (degenerative change), valve trauma (inf) ischemic change, congenital defects

44
Q

Damage to valves causes either

A

Stenosis: stiff valve, narrow orifice, flow impeded

Incompetence: distorted valves. Improper closure. Regurgitation

45
Q

Tx of valvular disease

A

Goal to maintain improve fx valves to prevent failure

Sx replacement

46
Q

5 steps in disease course

A 
Incubation 
Prodromal
Acute 
Convalescent 
Resolution

Patho (4 decks)

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